Stripping certain oral bacteria of their ac­cess key to gangs of other pathogenic oral bacteria could help prevent gum disease and tooth loss. A study published in the journal Microbiology suggests that this bacterial access key could be a drug target for people who are at high risk of developing gum disease. The bacteria Treponema denticola frequently gangs up in communities with other pathogenic oral bacteria to produce destructive dental plaque. Re­searchers from the University of Bristol have discovered that a molecule on the surface of T denticola called Trepo­nema denticola chymo­tryp­sin-like proteinase (CTLP) acts as the key pass that grants the bacterium access to the community by allowing it to latch onto other oral bacteria. Once incorporated, CTLP, in conjunction with other bacterial molecules, can start to wreak havoc by in­hibiting blood clotting (leading to continued bleeding of the gums) and causing tissue destruction. Pro­fessor Howard Jenkinson, who led the study, said that, “Devis­ing new means to control these infections requires deeper understanding of the microbes in­volved, their interactions, and how they are able to be­come incorporated into dental plaque.” The study shows that CTLP could be a good target from which novel therapies could be developed. He continued, “CTLP gives Trep­one­ma access to other periodontal communities, allowing the bacteria to grow and survive. In­hibiting CTLP would deny Trepo­nema access to the bacterial communities re­sponsible for dental plaque, which in turn would reduce bleeding gums and slow down the onset of perio­dontal disease and tooth loss.” The team is now working to find a compound that will inhibit CTLP. “If a drug could be developed to target this factor, it could be used in people who are at higher risk from developing gum disease,” explained Professor Jen­kinson. (Source: Society for Gen­eral Mi­cro­bi­ology, February 7, 2012. “Preven­t­ing bacteria from falling in with the wrong crowd could help stop gum disease.” Sci­ence­Daily. Re­trieved Febru­ary 9, 2012, sciencedaily.com)